Cardiac Valve Repair Device

Abstract

A cardiac valve repair device has a membrane assembly and a frame. The frame has a central structure that defines a central separation, a pair of sleeves positioned below the central structure, and a pair of atrial alignment expansion beams. Each atrial alignment expansion beam has a curved section and inner section at each opposite end that defines a scissor-crossing where they overlap each other to form a separate lower expansion clip beam at each of the opposite ends thereof. The cardiac valve repair device also includes a pair of upper expansion clip beams. A V-shaped ventricular expansion curved beam extends below the two sleeves, with the membrane assembly secured to the V-shaped ventricular expansion curved beam. A pair of ventricular alignment stabilizing beams extends downwardly from the two sleeves.

Description

RELATED CASES[0001]This is a continuation-in-part of Ser. No. 14 / 569,385, filed Dec. 12, 2014, and claims priority from 61 / 915,091, filed Dec. 12, 2013, both of whose disclosures are incorporated by this reference as though set forth fully herein.BACKGROUND OF THE INVENTION[0002]1. Field of the Invention[0003]The present invention generally relates to apparatus and methods for performing surgical, transcatheter or minimally invasive repair of a defective cardiac valve, such as the mitral, aortic, tricuspid and pulmonary valves.[0004]2. Description of the Prior Art[0005]The human heart has four major valves which moderate and direct blood flow in the cardiovascular system. These valves assure a unidirectional flow of blood supply through the cardiovascular system. Whereas the aortic, pulmonary, and tricuspid valves have three leaflets, the mitral valve has only two leaflets. The mitral valve and aortic valve control the unidirectional flow of oxygen-rich blood from the lungs to the b...

AI Technical Summary

Benefits of technology

The present invention provides a cardiac valve repair device that can be suspended within the flow path of a defective cardiac valve to reduce the prolapsed segment of the native valve leaflets, while retaining much of the native valve's structure and function. This device can improve functioning of the native valve by reducing the upward travel of the prolapsed segment of the native leaflets.

Problems solved by technology

Congenital, inflammatory, infectious conditions or diseases may lead to dysfunction of the valves over time.

Such degradation may result in serious cardiovascular compromise or even death.

The mitral valve and the aortic valve which are subjected to the systemic circulation high pressure generated by the left ventricle are more susceptible to dysfunction, such as stenosis or regurgitation.

For example, a stenotic mitral valve may impede blood flow into the heart, causing blood to back up and pressure to build in the lungs.

Regurgitation occurs when the mitral valve leaflets do not coapt correctly, thus causing blood to leak backwards into the left atrium and lungs each time the heart pumps.

Although the heart may gradually compensate for this overload as the leakage progresses slowly through months and years, the heart will eventually begin to fail.

All current valve prostheses have disadvantages, such as need for long-term maintenance with blood thinners, the risk of clot formation, limited durability, etc.

Today, standard valve replacement or repair procedure still requires an open-heart surgery which is prone to many complications and long hospital stays for recuperation.

The expanded prosthetic valve pushes the native valve leaflets aside and renders them ineffective.

Because the clip transforms the mitral orifice into two orifices, the clip may significantly obstruct the flow of blood through the valve.

The native structures of the mitral valve apparatus (mitral annulus and leaflets, chordae, papillary muscles, etc.) play an important role in left-ventricular function and therefore any valve replacement system that does not respect these elements may adversely impact the left-ventricular function.

This immobilizes the native leaflets, exerts tension to the chordae, and impairs the native function of the annulus, which can result in left-ventricular outflow tract (LVOT) obstruction and systolic anterior motion (SAM), etc.

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